The overall goal of this project is to test the hypothesis that oxidative stress plays a pathogenic role in preeclampsia. Dr. Robert's hypothesis is that abnormal placentation leads to relative ischemia and hypoxia, which then contributes to the generation of oxidative stressors in the maternal circulation that damage endothelium and lead to the widespread, multisystemic manifestations of preeclampsia. A second hypothesis is that maternal factors, which vary from woman to woman are important in the expression of the disease. The specific maternal factors to be explored are those that have also been associated with cardiovascular disease in nonpregnant populations; specifically, insulin resistance and dyslipidemia. The longitudinal data will be obtained from nulliparous women early in pregnancy, prior to disease, during disease, and postpartum. Using this strategy, various markers of oxidative stress in plasma/serum will be analyzed maternal and placental tissues will be examined for evidence of free radical induced damage the maternal constitutional factors contributing to oxidative stress will be examined and specific oxidative stressors will be studied such as TNF alpha, iron metabolism and consumption of ascorbate. Finally, the endogenous protective mechanisms against oxidative stress - antioxidants - will be measured.